Caloric restriction following early-life high fat-diet feeding represses skeletal muscle TNF in male rats

2021 ◽  
Vol 91 ◽  
pp. 108598
Author(s):  
Diego Hernández-Saavedra ◽  
Laura Moody ◽  
Xinyu Tang ◽  
Zachary J. Goldberg ◽  
Alex P. Wang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Caloric Restriction ◽  
High Fat Diet ◽  
Early Life ◽  
Male Rats ◽  
High Fat

scholarly journals A Memory of Early Life Physical Activity Is Retained in Bone Marrow of Male Rats Fed a High-Fat Diet

2017 ◽  
Vol 8 ◽  
Author(s):  
Dharani M. Sontam ◽  
Mark H. Vickers ◽  
Elwyn C. Firth ◽  
Justin M. O'Sullivan
Keyword(s):  
Physical Activity ◽  
Bone Marrow ◽  
High Fat Diet ◽  
Early Life ◽  
Male Rats ◽  
High Fat

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

2007 ◽  
Vol 293 (1) ◽  
pp. E31-E41 ◽  
Author(s):  
Robert C. Noland ◽  
John P. Thyfault ◽  
Sarah T. Henes ◽  
Brian R. Whitfield ◽  
Tracey L. Woodlief ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Weight Gain ◽  
High Fat Diet ◽  
Oxidative Capacity ◽  
Male Rats ◽  
High Fat ◽  
Endurance Running ◽  
Muscle Oxidative Capacity ◽  
Obesity And Diabetes

Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)- and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance.

scholarly journals Early life fluoxetine treatment causes long-term lean phenotype in skeletal muscle of rats exposed to maternal lard-based high-fat diet

2020 ◽  
Vol 131 ◽  
pp. 110727
Author(s):  
Diego Bulcão Visco ◽  
Raul Manhães-de-Castro ◽  
Márcia Maria da Silva ◽  
Jakssuel Sebastion Dantas-Alves ◽  
Bárbara J.R. Costa-de-Santana ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Fat Diet ◽  
Early Life ◽  
High Fat ◽  
Fluoxetine Treatment

scholarly journals Chronic AMP-activated protein kinase activation and a high-fat diet have an additive effect on mitochondria in rat skeletal muscle

2010 ◽  
Vol 109 (2) ◽  
pp. 511-520 ◽  
Author(s):  
Natasha Fillmore ◽  
Daniel L. Jacobs ◽  
David B. Mills ◽  
William W. Winder ◽  
Chad R. Hancock
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
High Fat Diet ◽  
Chemical Activation ◽  
Additive Effect ◽  
Male Rats ◽  
Fiber Types ◽  
High Fat ◽  
Rat Skeletal Muscle ◽  
Amp Activated Protein Kinase

Factors that stimulate mitochondrial biogenesis in skeletal muscle include AMP-activated protein kinase (AMPK), calcium, and circulating free fatty acids (FFAs). Chronic treatment with either 5-aminoimidazole-4-carboxamide riboside (AICAR), a chemical activator of AMPK, or increasing circulating FFAs with a high-fat diet increases mitochondria in rat skeletal muscle. The purpose of this study was to determine whether the combination of chronic chemical activation of AMPK and high-fat feeding would have an additive effect on skeletal muscle mitochondria levels. We treated Wistar male rats with a high-fat diet (HF), AICAR injections (AICAR), or a high-fat diet and AICAR injections (HF + AICAR) for 6 wk. At the end of the treatment period, markers of mitochondrial content were examined in white quadriceps, red quadriceps, and soleus muscles, predominantly composed of unique muscle-fiber types. In white quadriceps, there was a cumulative effect of treatments on long-chain acyl-CoA dehydrogenase, cytochrome c, and peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) protein, as well as on citrate synthase and β-hydroxyacyl-CoA dehydrogenase (β-HAD) activity. In contrast, no additive effect was noted in the soleus, and in the red quadriceps only β-HAD activity increased additively. The additive increase of mitochondrial markers observed in the white quadriceps may be explained by a combined effect of two separate mechanisms: high-fat diet-induced posttranscriptional increase in PGC-1α protein and AMPK-mediated increase in PGC-1α protein via a transcriptional mechanism. These data show that chronic chemical activation of AMPK and a high-fat diet have a muscle type specific additive effect on markers of fatty acid oxidation, the citric acid cycle, the electron transport chain, and transcriptional regulation.

Impact of high-fat diet and antioxidant supplement on mitochondrial functions and gene transcripts in rat muscle

2002 ◽  
Vol 282 (5) ◽  
pp. E1055-E1061 ◽  
Author(s):  
R. Sreekumar ◽  
J. Unnikrishnan ◽  
A. Fu ◽  
J. Nygren ◽  
K. R. Short ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Free Radical ◽  
Stress Response ◽  
High Fat Diet ◽  
Male Rats ◽  
High Fat ◽  
Antioxidant Supplementation ◽  
Transcript Levels ◽  
Atp Production ◽  
Mitochondrial Functions

High-fat diets are reported to increase oxidative stress in a variety of tissues, whereas antioxidant supplementation prevents many diseases attributed to high-fat diet. Rodent skeletal muscle mitochondrial DNA has been shown to be a potential site of oxidative damage. We hypothesized that the effects of a high-fat diet on skeletal muscle DNA functions would be attenuated or partially reversed by antioxidant supplementation. Gene expression profiling and measurement of mitochondrial ATP production capacity were performed in skeletal muscle from male rats after feeding one of three diets (control, high-fat diet with or without antioxidants) for 36 wk. The high-fat diet altered transcript levels of 18 genes of 800 surveyed compared with the control-fed rats. Alterations included reduced expression of genes involved in free-radical scavenging and tissue development and increased expression of stress response and signal transduction genes. The magnitude of these alterations due to high-fat diet was reduced by antioxidant supplementation. Real-time PCR measurements confirmed the changes in transcript levels of cytochrome c oxidase subunit III and superoxide dismutase-1 and -2 noted by microarray approach. Mitochondrial ATP production was unaltered by dietary changes or antioxidant supplemention. It is concluded that the high-fat diet increases the transcription of genes involved in stress response but reduces those of free-radical scavenger enzymes, resulting in reduced DNA repair/metabolism (increased DNA damage). Antioxidants partially prevent these changes. Mitochondrial functions in skeletal muscle remain unaltered by the dietary intervention due to many adaptive changes in gene transcription.

scholarly journals Perturbation of Hypothalamic MicroRNA Expression Patterns in Male Rats After Metabolic Distress: Impact of Obesity and Conditions of Negative Energy Balance

Endocrinology ◽  
2014 ◽  
Vol 155 (5) ◽  
pp. 1838-1850 ◽  
Author(s):  
Susana Sangiao-Alvarellos ◽  
Lara Pena-Bello ◽  
María Manfredi-Lozano ◽  
Manuel Tena-Sempere ◽  
Fernando Cordido
Keyword(s):  
Energy Balance ◽  
Caloric Restriction ◽  
Mirna Expression ◽  
High Fat Diet ◽  
Expression Profiles ◽  
Expression Patterns ◽  
Male Rats ◽  
High Fat ◽  
Peripheral Tissues ◽  
The Impact

The hypothalamus plays a crucial role in body weight homeostasis through an intricate network of neuronal circuits that are under the precise regulation of peripheral hormones and central transmitters. Although deregulated function of such circuits might be a major contributing factor in obesity, the molecular mechanisms responsible for the hypothalamic control of energy balance remain partially unknown. MicroRNAs (miRNAs) have been recognized as key regulators of different biological processes, including insulin sensitivity and glucose metabolism. However, the roles of miRNA pathways in the control of metabolism have been mostly addressed in peripheral tissues, whereas the potential deregulation of miRNA expression in the hypothalamus in conditions of metabolic distress remains as yet unexplored. In this work, we used high-throughput screening to define to what extent the hypothalamic profiles of miRNA expression are perturbed in two extreme conditions of nutritional stress in male rats, namely chronic caloric restriction and high-fat diet–induced obesity. Our analyses allowed the identification of sets of miRNAs, including let-7a, mir-9*, mir-30e, mir-132, mir-145, mir-200a, and mir-218, whose expression patterns in the hypothalamus were jointly altered by caloric restriction and/or a high-fat diet. The predicted targets of these miRNAs include several elements of key inflammatory and metabolic pathways, including insulin and leptin. Our study is the first to disclose the impact of nutritional challenges on the hypothalamic miRNA expression profiles. These data will help to characterize the molecular miRNA signature of the hypothalamus in extreme metabolic conditions and pave the way for targeted mechanistic analyses of the involvement of deregulated central miRNAs pathways in the pathogenesis of obesity and related disorders.

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